Tomato plant growth promotion and drought tolerance conferred by three arbuscular mycorrhizal fungi is mediated by lipid metabolism.

Arbuscular mycorrhizal fungi (AMF) can promote plant growth and enhance plant drought tolerance with varying effect size among different fungal species. However, the linkage between the variation and the lipid metabolism, which is exclusively derived from plants, has been little explored thus far. Here, we established AM symbiosis between tomato (Solanum lycopersicum) plants and three AMF species (Rhizophagus intraradices, Funneliformis mosseae, Rhizophagus irregularis) under well watered (WW) or drought stressed (DS) conditions in pot experiment. The plant biomass, chlorophyll fluorescence Fv/Fm, shoot P content and mycorrhizal colonization were determined. Meanwhile, fatty acid (FA) profiles and relative expression of genes encoding for nutrition exchange (SlPT4, SlPT5, RAM2, STR/STR2) in roots were also monitored. DS significantly decreased plant biomass while AMF significantly increased it, with three fungal species varying in their growth promoting capacity and drought tolerance capacity. The growth promoting effect of R. irregularis was lower than those of R. intraradices and F. mosseae, and was associated with higher mycorrhizal colonization and more consumption of lipids. However, the drought tolerance capacity of R. irregularis was greater than those of R. intraradices and F. mosseae, and was associated with less decrease in mycorrhizal colonization and lipid content. We also found that AMF mediated plant drought tolerance via regulating both AM specific FAs and non-AM specific FAs in a complementary manner. These data suggest that lipid metabolism in AM plays a crucial role in plant drought tolerance mediated by AMF.

Potential functions of the shared bacterial taxa in the citrus leaf midribs determine the symptoms of Huanglongbing.

Instruction: Citrus is a globally important fruit tree whose microbiome plays a vital role in its growth, adaptability, and resistance to stress. Methods: With the high throughput sequencing of 16S rRNA genes, this study focused on analyzing the bacterial community, especially in the leaf midribs, of healthy and Huanglongbing (HLB)-infected plants. Results: We firstly identified the shared bacterial taxa in the midribs of both healthy and HLB-infected plants, and then analyzed their functions. Results showed that the shared bacterial taxa in midribs belonged to 62 genera, with approximately 1/3 of which modified in the infected samples. Furthermore, 366 metabolic pathways, 5851 proteins, and 1833 enzymes in the shared taxa were predicted. Among these, three metabolic pathways and one protein showed significant importance in HLB infection. With the random forest method, six genera were identified to be significantly important for HLB infection. Notably, four of these genera were also among the significantly different shared taxa. Further functional characterization of these four genera revealed that Pseudomonas and Erwinia likely contributed to plant defense against HLB, while Streptomyces might have implications for plant defense against HLB or the pathogenicity of Candidatus Liberibacter asiaticus (CLas). Disccusion: Overall, our study highlights that the functions of the shared taxa in leaf midribs are distinguished between healthy and HLB-infected plants, and these microbiome-based findings can contribute to the management and protection of citrus crops against CLas.

Amelioration of Alcoholic Liver Steatosis by Dihydroquercetin through the Modulation of AMPK-Dependent Lipogenesis Mediated by P2X7R-NLRP3-Inflammasome Activation.

Dihydroquercetin (TAX) is the most abundant dihydroflavone found in onions, milk thistle, and Douglas fir bark. We investigated whether TAX could inhibit lipid accumulation in alcoholic liver steatosis in vivo and in vitro. An in vivo model was established by intragastrically treating mice with ethanol, and an in vitro model was created by treating HepG2 cells with ethanol. TAX regulated SREBP1 and ACC expression by elevating LKB1 and AMPK phosphorylation. Also, TAX upregulated SIRT1 expression, which was suppressed by ethanol intake. Decreased expression of P2X7R and NLRP3 and suppressed cleavage of caspase-1 by TAX resulted in the inhibition of IL-1ß production and release. Additionally, TAX reduced lipogenesis and promoted lipid oxidation via the regulation of AMPK and ACC in ethanol-treated steatotic HepG2 cells. TAX downregulated IL-1ß cleavage responses to LPS and ATP stimulation in HepG2 cells. P2X7R deficiency attenuated lipid accumulation, characterized by increased AMPK activity and decreased SREBP1 expression in ethanol-treated HepG2 cells. Our data showed that TAX exhibited the ability to inhibit lipogenesis and a hepatoprotective capacity, indicating that TAX has therapeutic potential for preventing alcoholic liver steatosis.

Liver kinase B1/AMP-activated protein kinase-mediated regulation by gentiopicroside ameliorates P2X7 receptor-dependent alcoholic hepatosteatosis.

BACKGROUND AND PURPOSE: Regulating P2X7 receptor-mediated activation of NLRP3 inflammasomes could be a therapeutic strategy to treat alcoholic hepatosteatosis. We investigated whether this process was modulated by gentiopicroside, the main active secoiridoid glycoside from Gentiana manshurica Kitagawa. EXPERIMENTAL APPROACH: In vivo models of acute and chronic alcoholic hepatosteatosis were established by intragastrically administered ethanol or using chronic plus binge ethanol feeding of Lieber-DeCarli liquid diet to male C57BL/6 mice. In vitro, HepG2 cells were treated with ethanol. RAW 264.7 macrophages and murine bone marrow-derived macrophages (BMDMs) were stimulated with LPS and ATP. KEY RESULTS: In both the acute and chronic alcohol-induced mouse hepatosteatosis models, gentiopicroside decreased serum aminotransferases and triglyceride accumulation. Up-regulated SREBP1, down-regulated PPARα and phosphorylated acetyl-CoA carboxylase caused by acute and chronic alcohol feeding were modulated by gentiopicroside, through the elevation of LKB1 and AMPK. Suppression of P2X7 receptor-NLRP3 activation by gentiopicroside inhibited IL-1ß production. In ethanol-exposed HepG2 cells, gentiopicroside reduced lipogenesis and promoted lipid oxidation via activation of P2X7 receptor-NLRP3 inflammasomes. Genetic or pharmacological blockade of P2X7 receptors enhanced AMPK activity and reduced SREBP1 expression in ethanol-treated HepG2 cells. Gentiopicroside down-regulated P2X7 receptor-mediated inflammatory responses in LPS/ATP-stimulated RAW 264.7 macrophages and BMDMs. IL-1ß from macrophages accelerated lipid accumulation in hepatocytes. Depleting macrophages by clodronate liposomes ameliorated alcoholic hepatosteatosis, and it was further alleviated by gentiopicroside. CONCLUSIONS AND IMPLICATIONS: Activation of LKB1/AMPK signalling by gentiopicroside was mediated by the P2X7 receptor-NLRP3 inflammasome, suggesting the therapeutic value of blocking P2X7 receptors in the treatment of alcoholic hepatosteatosis.

Oligomeric proanthocyanidin derived from grape seeds inhibited NF-κB signaling in activated HSC: Involvement of JNK/ERK MAPK and PI3K/Akt pathways.

In current study, we aimed to reveal the potential antifibrotic effects of oligomeric proanthocyanidin (OPC) from grape seeds on lipopolysaccharide (LPS)-activated, HSC-T6, a rat hepatic stellate cell line. HSC-T6 cells were treated with OPC 1h prior to LPS, and then incubated for indicated time. OPC inhibited cells viability of HSC-T6 cells and decrease protein expression of collagen I, α-smooth muscle actin (α-SMA), tissue inhibitors of metalloproteinases I (TIMP-1) on LPS-induced HSC-T6 cells. OPC also significantly inhibited phosphorylation of LPS-stimulated phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). Furthermore, OPC pretreatment blocked LPS-triggered nuclear factor-kappa B (NF-κB) translocation from cytosol to nuclear. OPC, as well as specific inhibitors of NF-κB, PI3K and JNK could effectively inhibited α-SMA and collagen I expression. In conclusion, we demonstrated that the anti-fibrotic mechanism of OPC might be involved the inhibition of HSC activation and transdifferentiation by suppressing NF-κB activation through JNK/ERK MAPK and PI3K/Akt phosphorylation. Thus, OPC possesses the potential inhibitory property of HSC activation through NF-κB modulation involving MAPK-PI3K/AKT pathways.